目的：探讨高迁移率蛋白B1（HMGB1）促进血管平滑肌细胞（VSMC）增殖与迁移的机制。 方法：检测人主动脉血管平滑肌细胞（HA-VSMC）与HMGB1 孵育后增殖与迁移的活性、晚期糖基化 终产物受体（RAGE）与P38MAPK 表达改变，以及RAGE 抗体、P38MAPK 抑制剂SB203580 预处理 的影响。 结果：HMGB1 孵育后，HA-VSMC 增殖与迁移活性、RAGE 和P38MAPK 的表达均明显增加（ 均 P<0.05），且均呈一定的浓度依赖性。用RAGE 抗体和SB203580 预处理后，HMGB1 促进HA-VSMC 增殖及迁移的作用均被明显抑制（均P<0.05），RAGE 抗体预处理后，HMGB1 对P38MAPK 表达的诱 导作用明显抑制（P<0.05）。 结论：HMGB1 可能通过与细胞表面RAGE 受体结合，激活P38MAPK 表达进而促进VSMC 的增殖及迁移。
Mechanism for HMGB1 in promoting migration and proliferation of vascular smooth muscle cells
Objective: To investigate the mechanism of high mobility of protein B1 (HMGB1) in promoting migration and proliferation of vascular smooth muscle cells (VSMCs). Methods: The changes in migration and proliferation ability as well as the expressions of receptor for advanced glycation end-products (RAGE) and P38MAPK were measured in human aortic VSMCs (HA-VSMCs) after exposure to HMGB1. Further, the influence of RAGE antibody or P38MAPK inhibitor SB203580 pretreatment was observed. Results: After exposure to HMGB1, the activity of the cell proliferation and migration, as well as the expression of RAGE and P38MAPK were increased significantly (all P<0.05), and all presented in a concentration-dependent manner. The promoting effects of HMGB1 on migration and proliferation ability were significantly inhibited by either RAGE antibody or SB203580 pretreatment (all P<0.05), and HMGB1-induced P38MAPK expression was significantly inhibited by RAGE antibody pretreatment (P<0.05). Conclusion: HMGB1 can probably promote the migration and proliferation of VSMCs through its binding to cell surface RAGE and then activating P38MAPK expression.